A popular, but still unproven, hypothesis about hypertension is that intermittent increases in sympathetic vasomotor activity elicit pressor responses which though initially transient, later become sustained. Strongly supporting this hypothesis is Folkow and Rubinstein's finding that in awake rats, systolic pressure (measured indirectly once a week using the tail-cuff method) is moderately increased by chronic electrical stimulation of the hypothalamus. We propose to re-examine this problem by using methods we have developed for measuring arterial pressure directly from chronically-implanted catheters. Indwelling flow probes will also be implanted around the ascending aorta to allow recording of changes in cardiac output and peripheral resistance. Instead of relying on hypothalamic stimulation alone, our studies will explore the possibility that sustained hypertension results from chronic exposure to a combination of predisposing factors. Because cardiovascular function is normally regulated by the sympathetic nervous system, our working hypothesis assumes that the primary disturbance in hypertension is one of sympathetic overactivity. Based on the known interaction between the sympathetic nervous system and other organs, initial attempts to produce hypertension will combine continuous electrical stimulation of hypothalamic vasomotor centers with change in salt intake, or renal or adrenocortical function.